From Volume 48, Issue 1, January 2021 | Pages 54-57
Cerebral abscesses of odontogenic origin are uncommon. Cerebral abscesses are often caused by cardiac and pulmonary disease or infections such as skin or abdominal infections. However, there have been some reported incidences of cerebral abscesses caused by odontogenic infection. This paper aims to discuss a case report whereby an odontogenic infection was the most probable cause of a cerebral abscess in a paediatric patient.
Cerebral abscesses secondary to odontogenic infection are rare. Previous publications tend to be case reports of a single patient, such as the example reported by Corson et al in 2001.1 There are three main routes by which a bacterial odontogenic infection can enter the brain: the paranasal sinuses; the oropharynx: and the middle ear.2 A cerebral abscess can be a life-threatening condition, which needs to be managed quickly and efficiently. Diagnosis of a cerebral abscess can be challenging as presentation is variable in patients. Thus, it is important to understand that clinical suspicion is of merit in these situations and can aid a quicker diagnosis.3 Patients commonly present with headaches, nausea/vomiting and fever.3 It has been reported that seizures can occur as well as neck stiffness, speech and vision problems. All of these symptoms are suggestive of focal neurological deficits.3,4
In order to diagnose a cerebral abscess, blood cultures and brain imaging can be used. In a small number of patients, leukopenia can be present and, therefore, taking blood cultures early is of benefit. MRI scans and CT scans with contrast are also invaluable; however, MRI scans have greater sensitivity and specificity compared to a CT scan when detecting pyogenic infection. As a consequence an MRI scan is the imaging of choice.3 An urgent MRI scan may not be available, therefore diagnosis is commonly made from a contrasted CT scan instead. Imaging from an MRI scan can be improved through the use of perfusion, diffusion and magnetic resonance spectroscopy. These techniques are useful when aiming to differentiate an infection from a neoplastic lesion as discussed by Hakim et al.5
There are various causes for a cerebral abscess and include neurosurgical procedures, traumatic injuries, paranasal sinus infection and dental infection.3 Therefore, when managing a cerebral abscess, it is important to not only understand the main cause, but also exclude other possible causes. This case report aims to highlight the importance of investigating odontogenic infection.
A 12-year-old boy attended Great Ormond Street Hospital as an emergency for a large left temporal brain abscess. The patient had several comorbidities including autism, short stature, complex congenital heart disease and a sleep disorder. He initially presented to his local hospital with a 1-week history of malaise and lethargy. There was a 3-day history of fever, headache, painful neck and back, and eye pain. On examination the patient had radiographic changes visible on his chest radiograph that appeared to be consistent with pneumonia. From this, the initial impression was that he had a lower respiratory tract infection. The patient was subsequently admitted and placed on intravenous antibiotics (ceftriaxone and meropenem) and the antiviral medication, oseltamivir. However, he continued to have severe headaches and neck pain. His systemic temperature showed paroxysmal elevation during the night and he became disorientated with neurological signs of ongoing severe headaches and confusion. A CT scan was performed, showing a large left temporal lobe abscess and an adjacent small abscess (Figure 1). There was also dilatation of the right lateral ventricle. This appearance was of a left temporal lobe cerebral abscess with secondary ventriculitis and obstructive hydrocephalus of the right lateral ventricle.
The patient was urgently transferred to the neurosurgery unit at Great Ormond Street Hospital for treatment. Owing to the proximity of the cerebral abscess to the ipsilateral mastoid air space, the ear nose and throat team were consulted and they decided to perform a mastoid washout under the same anaesthetic. The patient underwent emergency surgery comprising neuronavigation-guided burr hole aspiration of the abscess. The mastoid washout did not reveal pus in the antrum. Samples of tissue were sent to the laboratory for microbiological investigation. The final bacteria isolated was Streptococcus intermedius and Paenibacillus. Antimicrobial management was changed from intravenous meropenem to cefotaxime and oral metronidazole with a plan to continue for a minimum of 6 weeks.
As part of the investigation into the cause of the temporal lobe abscess, the paediatric dental team at Great Ormond Street Hospital received a referral from the neurosurgery team to undertake a dental examination to consider a potential oral cause for the temporal abscess. The patient attended the dental department less than 24 hours after surgery. A full clinical and radiographic examination was carried out. The patient was in the permanent dentition with no evidence of dental caries but very poor oral hygiene. Generalized plaque and calculus deposits were present throughout his mouth. The soft tissues, particularly the gingivae were inflamed, erythematous and suppuration palatal to the maxillary right central incisor was noted. An OPG radiograph was taken on the day of the dental review (Figure 2). This film confirmed the clinical finding that the patient was caries free and bone levels were within normal limits. The patient had a complete developing permanent dentition including unerupted third permanent molars consistent with his age. However, above the maxillary right third molar, a well corticated circular lesion appeared to be present. The maxillary left central incisor also appeared to have reduced root length. An upper standard occlusal radiograph was taken to investigate this and, while the maxillary left central incisor was shown to have normal root length, there appeared to be peri-apical pathology of the maxillary right lateral incisor (Figure 3).
Subsequently, an urgent referral was sent to a consultant dental radiologist to interpret the findings of the radiographs, but who considered the OPG to be suboptimal with rotation and positioning errors, making bilateral comparison challenging. Initial report of the OPG suggested that the left maxillary antrum was hypoplastic, or absent, and the right antrum was likely to be septated. The radiologist reported no abnormal findings on the upper standard occlusal radiograph and stated that normal anatomy was present. Peri-apical radiographs of the maxillary anterior teeth were taken to confirm no peri-apical pathology was present (Figure 4). This illustrated the importance of ensuring correct positioning prior to obtaining radiographs.
Intra-oral photographs, which had not been possible at initial presentation, were obtained after 1 week, when some healing had already taken place. The lesion palatal to UR1 was still visible as noted (Figure 5) and generalized gingival inflammation was also still evident as shown in a left buccal view of the dentition (Figure 6). From the findings above, the main concern was in relation to the intra-oral soft tissues. The generalised inflammation and suppuration present led to the initial diagnosis of a periodontal condition, acute necrotizing ulcerative gingivitis (ANUG), being a potential source of oral infection responsible for the brain abscess.
In the literature, there have been cases of periodontal disease causing intracranial abscesses. Brady et al discussed a case of Aggregatibacter actinomycetemcomitans being an important pathogen in the cause of a brain abscess in a patient with a poor dentition.6 Moreover in 2011, Rahamat-Langendoen described a case of a brain abscess associated with A. actinomycetemcomitans in a patient with a poor dentition.7 Consequently, a mouth swab was taken from the patient and results returned as normal. As the patient had already been prescribed antibiotics, including metronidazole, by medical professionals, the dental team arranged for a full mouth supragingival debridement to be carried out. Tailored oral hygiene instruction was also given and a 1-month follow-up with the dental team was arranged.
The patient was reviewed 1 month later in the dental department at Great Ormond Street Hospital by the paediatric dental team. Following a review and a second course of supragingival debridement, the gingival inflammation had improved. There was no evidence of suppuration of the incisive papillae and the area had healed well. However, the patient's oral hygiene was still in need of improvement because marginal gingivitis was still evident. The patient was to return to the dental department 1 month later for a course of supra- and subgingival debridement before being put on 3-monthly recalls with the hygienist, and a 6-monthly review with the paediatric dental team. From a neurological perspective, imaging was reviewed and the post-operative abscess had improved. The patient was well with no neurological deficit. A comparison of MRI scans taken in April and May 2019 showed resolving infection and no evidence of venous thrombosis (Figure 7a,b). The patient had stopped taking antibiotics and remained well. A follow up MRI scan 3 months later was planned.
There exist multiple causes of intracranial abscesses. In this case, the diagnosis of periodontal disease causing the large left temporal brain abscess was made. No other cause was identified on routine investigation. However, as much as this was a diagnosis of exclusion, there does appear to be evidence in this case that the patient's ongoing periodontal disease was the cause of the cerebral abscess.
While this case report discusses periodontal disease as a diagnosis of exclusion, there are cases in the literature of cerebral abscesses being caused by periodontal disease. For example, Rae Yoo et al reported a rare case of Porphyromonas gingivalis being the cause of a brain abscess.9 They reported that, for a brain abscess to have an odontogenic cause, there are three main factors involved. First, there has to be no other source of bacterium that may have caused the brain abscess. Secondly, there has to be clinical evidence of periodontal disease and thirdly, there must be oral microflora detected during investigations.9 Another case reported a 65-year-old male patient who developed a right frontal brain abscess, with the pathogen P. gingivalis being the sole bacterial cause of the abscess.10 While this case report aims to highlight odontogenic infection as a potential causative factor for a cerebral abscess, the authors do acknowledge that there are very few cases of periodontal disease being a causative factor for a brain abscess in the literature. However, even with such few cases, it is important to note that there was a correlation between periodontal disease and cerebral infection.
In conclusion, this case report has highlighted the importance of identifying oral disease as a potential source of cerebral infection. Dental professionals should be aware of the potential dangers of untreated dental disease, including periodontal disease as a causative factor for a brain abscess. This report emphasizes the importance of multidisciplinary care in understanding the causes of cerebral infection. It was also complicated by the fact that the patient had autism and was unable either to assist with imaging in a timely manner or maintain good oral hygiene. The role of his parents in the latter has been emphasized. Therefore, in patients with poor oral health, every effort should be made to investigate dental infection as a possible cause for a cerebral abscess.
